The mechanisms involved in the immunopathogenesis of experimental allergic uveitis (EAU) induced by rhodopsin in mycobacterial adjuvant sensitization of guinea pigs will be defined to provide approaches for understanding the role of autoimmunity in initiation and propagation of human ocular diseases. Our objectives will be: 1) Delinecte the role of the lymphocyte in autoimmunity. Specific projects are proposed which deal with exploring variables for production of an idealized model of EAU; immunohistopathologic temporal studies to document the time course of retinal destruction of the cellular level, as well as localization of specific autoantigens in ocular tissues and temporal studies of the role of cell-mediated immunity (CMl) and of autoantibody in initiation and propagation of disease; and passive transfer studies of the role of T and B lymphocytes in production of EAU. 2) Manipulate the immune response of EAU afflicted animals to assess the therapeutic potential of immunologic intervention. Explore various regimens employing antigen presensitization, antigen desensitization after disease induction, mycobacterial adjuvant presensitization, T-cell depletion, and passive antibody in the model. 3) Evaluate the role of specific cell-mediated and humoral immune responses in the pathophysiology of human uveitis and retinitis by studies on lymphocyte functions and populations. Assess cellular reactivity of host lymphocytes to retinal and ocular tissue antigens by in vitro tests of CMl. Correlate of humoral immune response with the CMl and disease. The long term objective of our research is to apply the information gleaned by our studies to early diagnosis, modes of therapy, and optimal management of inflammatory autoallergic diseases affecting human vision.